--unexplained mild "LVH"
--PAF that has little explanation
--spinal stenosis
--carpal tunnel
--orthostatic hypotension
--bruising
--lack of EF response to #GDMTworks
--Diuretic sensitivity
--Higher biomarkers "than they should be"
Why are biomarkers higher in amyloid? It has mainly to do with direct myocardial toxicity of the amyloid protein, and NOT congestion/ischemia in most cases.
hs-cTn is almost universally elevated.
Both NPs and hs-cTn are prognostic, regardless of their 'decoupling' from HF/MI.
I have dx'd people without HF symptoms on the basis of some of the above findings.
Think of the diagnosis, because if you don't, you won't recognize it until it's later in the process.
This is important because treatments for ATTR are most effective EARLY in the disease course.
With other treatments coming, early and definitive diagnosis is really important.
Here's an intriguing analysis just published in Diabetes Care by the great folks at @AmDiabetesAssn and @ADA_Journals. We examined concentrations of insulin-like growth factor binding protein-7 (IGFBP7) at BL and 1Y in the CANVAS study.
Though IGFBP7 "looks like" an IGF binder, it is lousy at this job. But IGFBP7 has other roles: it is a cell cycle arrest biomarker in the 'senescence associated secretory phenotype'.
When cells are exposed to IGFBP7 in excess, fibrosis follows.
2/
We previously found IGFBP7 was associated with cardiac structural and functional abnormalities and outcome in patients with heart failure, but we were interested to see how it would act in patients with #T2D, such as those in CANVAS.
I just finished reading another poorly-composed position paper from a major society regarding COVID19 with recommendations based on a handful of sometimes questionable papers and have a few thoughts. 1)
The pandemic has put a terrible strain on everyone. It's been very, very difficult and very frightening. What some institutions went through will leave them scarred for years to come. All of this has left people hungry for high quality science informing treatment decisions. 2)
The desire for rapid data is understandable. But there's a dark side that many of us have observed: authors have rushed papers to publication that on any non-pandemic day would have been desk rejects, but in the current environment have been published in major/top journals. 3)
2/Why "trend troponin to peak" anyhow? Most do it to "size" the infarct; specifically, the concept is that the amount of troponin efflux from necrotic tissue is proportional to the size of the infarct.
But is this true? Is it accurate?
3/In a very nice review (karger.com/Article/Fullte…) Hallen makes the important point that infarct size and troponin kinetics ARE modestly correlated (r values of 0.5-0.75), BUT best data are with STEMI. We don't need troponins to diagnose or estimate infarct size in STEMI.